Aim: 

The nature of ROS/RNS involved in PostC triggering is unknown. Both ONOO^- and H₂O₂ have been proposed as possible candidates. To throw light on this issue we studied 1) the role of CAT and SOD and 2) the presence of nitrosylated proteins during reperfusion with or without PostC.

Methods: 

isolated rat hearts underwent 30-min ischemia/120-min reperfusion (I/R) only or PostC (5 cycles of 10-sec I/R at the beginning of 120-min reperfusion) either with or without CAT (100 U/ml) or SOD (10 U/ml) given during the early R. Heart samples collected at 7^th and 120^th min of R were used to study the activity of SOD and CAT and for the analysis of nitrosylated proteins. Infarct size (IS) was evaluated with nitroblue-tetrazolium staining.

Results: 

IS was similar (60-70% of risk area) in hearts subjected toI/R only either with or without CAT or SOD. PostC reduced IS to 33±5% and to 38±5% without and with CAT, respectively. Yet, SOD infusion abolished PostC protection (IS: 75±2%). While CAT activity was higher in the PostC than in I/R, the SOD activity was higher in I/R than PostC. PostC increased nytrosilated proteins.

Conclusions: 

PostC induces an up-regulation of CAT and a down-regulation of SOD. When SOD is infused less ONOO^- is formed and more H₂O₂ is produced and PostC cardioprotection is abolished; yet when CAT is infused PostC protection is not affected. It seems that H₂O₂ is not a trigger of PostC and ONOO^- is involved in PostC protection,